Progress on Hypoxic-ischemic Brain Damage Associated with CCR2 and CCL2.
- Author:
Yu-jia LUO
;
Ru-bo LI
;
Shi-yu MA
;
Meng-yan LÜ
- Publication Type:Review
- MeSH:
Animals;
Brain Injuries/pathology*;
Cerebral Cortex/physiopathology*;
Chemokine CCL2/metabolism*;
Chemokines, CC/metabolism*;
Hypoxia-Ischemia, Brain/metabolism*;
Macrophage Inflammatory Proteins/metabolism*;
RNA, Messenger/metabolism*;
Rats;
Rats, Sprague-Dawley;
Receptors, CCR2/metabolism*
- From:
Journal of Forensic Medicine
2016;32(1):54-57
- CountryChina
- Language:Chinese
-
Abstract:
Hypoxic-ischemic brain damage (HIBD) is referred to a common type of cerebral damage, which is caused by injury, leading to shallow bleeding in the cortex with intact cerebral pia mater. In recent years, studies show that a various kinds of immune cells and immune cellular factors are involved in the occurrence of HIBD. CC chemokine receptor 2 (CCR2) is a representative of CC chemokine receptor, and is widely distributed in cerebral neuron, astrocyte, and microglial cells, and is the main chemo-tactic factor receptor in brain tissue. CC chemokine ligand 2 (CCL2) is a kind of basophilic protein and the ligand of CCR2, and plays an important role in inflammation. In order to provide evidence for correlational studies in HIBD, this review will introduce the biological characteristics of CCR2 and CCL2, and illustrate the relationship between the immunoreactivity and HIBD.
